《毒理学》毒理学替代实验.ppt

There is the same in genetic and diference in reversible between the genetics and epigenetics. The gene mutation is not reversible, but the epigenetic variation is reversible. For example, the DNA base A become to T and it dosen't reverse T to A. However, the DNA can be methylated and be demethylated. Epigenetic variation is reversible. We wonder what is the relationship between the genomic damage and epigenetic expression? And the interaction between the genetics and epigenetics? How improve the risk assessment by exploring the mechanisms fo carcinogenesis? * * * The goal of toxicity testing should be to assess the likely risks posed to human populations at environmental exposure levels; that is (i.e.), provide the data necessary for a realistic assessment of human risk. The current approaches for assessing chemical toxicity mostly depend on animal test, which is time-consuming, elaborate and expensive. Obviously, the traditional methods do not meet the current demand. This expensive, low-throughput approach relies on conservative extrapolations to relate animal studies to much lower-dose human exposures and is of questionable relevance to predicting risks to humans at their typical low exposures. It makes little use of a mechanistic understanding of the mode of action by which chemicals perturb biological processes in human cells and tissues. It is urgent to develop alternative assays to predict the long-term effects such as carcinogenicity. In vitro methods that assess changes in biologic processes using primary cells, cell lines, or cellular components, preferably of human origin, in combination of high-throughput screening assays will allow us to test more chemicals at less cost. In response to these concerns, in 2004 the U.S. Environmental Protection Agency (U.S. EPA) and the National Toxicology Program of the U.S. National Institute of Environmental Health (NTP of U.S. NIEH) Sciences commissioned a committee of the National Academy of Sciences to evaluate cu